Photobiomodulation as a contemporary antioxidant intervention in myocardial infarction

Myocardial infarction (MI) triggers a complex cascade of structural and functional alterations that frequently culminate in adverse cardiac remodelling and heart failure. Central to this process is the excessive production of reactive oxygen species (ROS), which disrupt mitochondrial function, impair calcium handling, and activate pro-apoptotic and pro-fibrotic pathways. Photobiomodulation (PBM) has emerged as a non-invasive therapeutic approach capable of modulating several key biological processes involved in post-infarction remodelling. Preclinical studies consistently demonstrate that PBM reduces infarct size, attenuates ventricular dilation, and improves both systolic and diastolic function. Through the absorption of red to near-infrared light by mitochondrial chromophores, particularly cytochrome c oxidase, PBM enhances cellular bioenergetics, modulates ROS production and activates redox-sensitive signalling pathways. These effects promote a shift from detrimental oxidative stress toward controlled ROS signalling and, in turn, facilitate cytoprotective, anti-inflammatory and pro-angiogenic responses. In addition, PBM promotes the mobilization of progenitor cells, contributing to tissue repair and microvascular restoration. Although still limited, the available clinical evidence suggests that PBM may confer modest improvements in cardiac function. However, variability in treatment protocols, delivery methods and study designs currently precludes definitive conclusions regarding its clinical efficacy. In summary, PBM represents a promising strategy for modulating oxidative stress after MI, integrating metabolic, redox and signalling pathways to attenuate cardiac remodelling. Further well-designed clinical studies are required to establish standardized protocols and to clarify its therapeutic potential in cardiovascular medicine.